Macrophage Fc (IgG) and C3 receptors are important in host defense and in the pathophysiology of several immunologic disorders. Enhancement of their activity facilitates the ability of these cells to eliminate microorganisms while inhibition improves the clinical status of patients in several immunologic diseases. In the lung, the pulmonary macrophage (PAM) appears to have a similar functional role. Our goals in this proposal are to further characterize the Fc, C3 and fibronectin receptors on normal PAM. Furthermore, we will delineate mechanisms which modulate the expression of these recpetors and examine how these receptors differ among macrophage subpopulations. We will study Fc (IgG), C3 and fibronectin receptor expression among PAM subpopulations by analyzing the binding by PAM of 1) radiolabeled IgG and C3b monomer and oligomer and fibronectin monomer and 2) erythrocytes coated with defined amounts of IgG, and affinity of PAM binding sites for monomeric and oligomeric IgG. We will also examine the effect of Fc (IgG) receptor perturbation on the number and affinity of macrophage binding sites for C3b monomer and dimer. We will define the mechanisms by which a synthetic N-foryl ogiopeptide, similar to that produced by acteria, augments PAM Fc (IgG) receptor activity and determine its effect on C3b receptor expression. We will also analyze the effect of fibronectin on the expression of these surface receptors. We will determine the mechanisms by which corticosteriods, commonly utilized pharmacologic agents in pulmonary disease, modulate PAM Fc (IgG) and C3 receptor expression. We will examine the capacity of steriod analogues to enhance or inhibit the expression of these receptors. Since steriods may be administered locally to the lung, these studies may be of therapeutic importance. Finally, we will examine PAM from patients with pulmonary disease in which immunopathogenesis is of major importance. We will analyze PAM subsets in these patients for differences in receptor expression and modulation; such differences may be important contributing factors to the pathogensis of pulmonary disease.